TY - CHAP
T1 - Obstructive sleep apnea
AU - Pham, Luu V.
AU - Jun, Jonathan
AU - Polotsky, Vsevolod Y.
N1 - Publisher Copyright:
© 2022 Elsevier B.V.
PY - 2022/1
Y1 - 2022/1
N2 - Obstructive sleep apnea (OSA) is a disease that results from loss of upper airway muscle tone leading to upper airway collapse during sleep in anatomically susceptible persons, leading to recurrent periods of hypoventilation, hypoxia, and arousals from sleep. Significant clinical consequences of the disorder cover a wide spectrum and include daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease, metabolic dysfunction, respiratory failure, and pulmonary hypertension. With escalating rates of obesity a major risk factor for OSA, the public health burden from OSA and its sequalae are expected to increase, as well. In this chapter, we review the mechanisms responsible for the development of OSA and associated neurocognitive and cardiometabolic comorbidities. Emphasis is placed on the neural control of the striated muscles that control the pharyngeal passages, especially regulation of hypoglossal motoneuron activity throughout the sleep/wake cycle, the neurocognitive complications of OSA, and the therapeutic options available to treat OSA including recent pharmacotherapeutic developments.
AB - Obstructive sleep apnea (OSA) is a disease that results from loss of upper airway muscle tone leading to upper airway collapse during sleep in anatomically susceptible persons, leading to recurrent periods of hypoventilation, hypoxia, and arousals from sleep. Significant clinical consequences of the disorder cover a wide spectrum and include daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease, metabolic dysfunction, respiratory failure, and pulmonary hypertension. With escalating rates of obesity a major risk factor for OSA, the public health burden from OSA and its sequalae are expected to increase, as well. In this chapter, we review the mechanisms responsible for the development of OSA and associated neurocognitive and cardiometabolic comorbidities. Emphasis is placed on the neural control of the striated muscles that control the pharyngeal passages, especially regulation of hypoglossal motoneuron activity throughout the sleep/wake cycle, the neurocognitive complications of OSA, and the therapeutic options available to treat OSA including recent pharmacotherapeutic developments.
KW - Complications
KW - Pathogenesis
KW - Pharmacologic therapy
KW - Starling resistor
UR - http://www.scopus.com/inward/record.url?scp=85136556960&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85136556960&partnerID=8YFLogxK
U2 - 10.1016/B978-0-323-91532-8.00017-3
DO - 10.1016/B978-0-323-91532-8.00017-3
M3 - Chapter
C2 - 36031300
AN - SCOPUS:85136556960
T3 - Handbook of Clinical Neurology
SP - 105
EP - 136
BT - Handbook of Clinical Neurology
PB - Elsevier B.V.
ER -